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Suppression of Mitochondrial Permeability Transition Pore and Induction of Lymphoma P388 Cell Death by Cyclosporin A
Author(s) -
Teplova V.,
Evtodienko Yu.,
Odinokova I.,
Kruglov A.,
Kudrjavtsev A.
Publication year - 2000
Publication title -
iubmb life
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.132
H-Index - 113
eISSN - 1521-6551
pISSN - 1521-6543
DOI - 10.1080/15216540050176638
Subject(s) - mitochondrial permeability transition pore , programmed cell death , apoptosis , mitochondrion , chemistry , cell , lymphoma , cell culture , microbiology and biotechnology , biology , biophysics , stereochemistry , biochemistry , immunology , genetics
Suppression of the mitochondrial permeability transition pore (PTP) and induction of lymphoma P388 cell death were studied in the presence of cyclosporin A (CsA) and its derivatives. In experiments with permeabilized P388 cells, CsA and its nonimmunosuppressive derivative N‐methyl‐Val‐4‐CsA, but not cyclosporin H (CsH), enhanced Ca2+ accumulation in mitochondria and suppressed PTP opening. Moreover, CsA was able either itself to induce or to enhance a prooxidant‐induced P388 programmed cell death. Blebbing and formation of apoptotic bodies were among the observed CsA effects. N‐Methyl‐Val‐4‐CsA showed similar effects, but CsH had no effect on P388 cell death. These results show that initial‐stage P388 tumour cell death is not related to PTP opening but can be the result of PTP closing with a corresponding increase in the formation of reactive oxygen species.